Suicidal exposure

Carbon monoxide (CO) is a colorless, odorless gas that is ubiquitous because it is created whenever carbon-containing materials are burned. Carbon monoxide poisoning is the leading cause of death due to poisoning in the USA. Most cases occur in victims of fires, but accidental and suicidal exposures are also common. The diagnosis and treatment of carbon monoxide poisoning are described in Chapter 56. Many other toxic gases are produced in fires or released in industrial accidents (Table 58-5). 

Organophosphorus compounds and carbamates, also known more generally as cholinesterase inhibitors, are widely used pesticides that may cause poisonings after accidentai or suicidal exposure. Poisonings are particularly common in rural areas and third-world countries where more potent agents are widely available. Several chemical warfare agents (eg, GA [Tabun], GB [Sarin], GD [Soman], GF, and VX) are extremely potent cholinesterase inhibitors (see p 372 and Table 11-57). Household insect sprays often contain low-potency cholinesterase inhibitors. (Many commercial products also contain solvents such as toluene or xylene that can themselves produce toxic effects in an overdose see p 357). 

LD50 (oral, rat) > 505 mg/kg LCLo (inh., human, 30 min) 4000 ppm readily absorbed thru skin dissolves oils from skin splashes in eyes cause immediate severe irritation tumorigen inh. may cause severe personality disturbances, confusion, insomnia, psychosis, suicide exposure 4800 ppm for 30 min causes coma and may be fatal ing. may cause vomiting, diarrhea, headache, convulsions, coma, death toxic to reproduction TSCA listed... 

Domestic during either accidental or intentional suicidal exposure, ingestion in foods or as a toxic contaminant of food, exposure to toxic agents such as in the form of glue sniffing. 

The lymphocytes from 31 patients exposed to various organophosphate pesticides were examined for chromosomal aberrations (Van Bao et al. 1974). Five of the patients were exposed to methyl parathion only. Blood samples were taken 3-6 days after exposure and again at 30 and 180 days. A significant (p<0.05) increase was noted in the frequency of stable chromosomal aberrations in acutely intoxicated persons (although such cells are eventually lost from the cell population). Two of the methyl parathion-exposed persons had taken large doses orally in suicide attempts. The study limitations include small sample size, absence of a control group, lack of quantification of exposure levels, and possible... 

No data are available on platelet NTE activity in exposed subjects, and little data on lymphocyte NTE activity. In one reported case of suicidal poisoning with chlorpyrifos, inhibition of lymphocyte NTE was correlated with the enzyme inhibition in peripheral nerves (Osterloh et al., 1983). In another case of attempted suicide with the same compound, inhibition of NTE in peripheral lymphocytes was associated with the development of delayed neuropathy (Lotti, 1986). However, the threshold of NTE inhibition required for delayed neuropathy remains undetermined (Lotti, 1987). Observations in occupationally exposed subjects are limited in number, and more research is needed to investigate the applicability of NTE as a biomarker of exposure to OP pesticides. 

All fire smoke is toxic. In the past two decades, a sizable research effort has resulted in the development of over twenty methods to measure the toxic potency of those fire smokes (6). Some methods have been based on determinations of specific chemical species alone. Values for the effect (e.g., lethality) of these chemicals on humans are obtained from (a) extrapolation from preexisting, lower concentration human exposure data or from (b) interpretation of autopsy data from accident and suicide victims. The uncertainty in these methods is large since ... 

I felt like a magnet, like everything was coming off from other people onto me. I became suicidal and wanted to die. I took a bunch of pills and had to have my stomach pumped. I thought there was no help and no hope. That s when my family physician told me that he thought Dr. Erica Elliott could help me. My husband and brother went with me to see her. She told us she had an illness caused by exposure to chemicals, and that the same thing had happened to me. I was so relieved I cried. I was so happy to find out I wasn t crazy. 

Oral exposure to cyanide usually results from accidental, homicidal, or suicidal ingestion of cyanide salts. Sodium cyanide and potassium cyanide are the most frequently studied cyanide compounds. Copper cyanide, potassium silver cyanide, silver cyanide, and calcium cyanide are other compounds that humans could encounter through oral or dermal exposure. Cassava roots and certain fruit pits contain compounds that can be broken down to form cyanide. Cassava roots form the staple diet of some populations in Africa, Central and South America, and Asia. However, it must be noted that cassava roots are notoriously deficient in protein and other nutrients and contain many other compounds, in addition to cyanide, that could be responsible for some of the observed toxic effects. Thiocyanate is a metabolite of cyanide that is formed in the body after exposure to cyanide compounds. When possible, all oral exposures are expressed as mg CN/kg/day. 

One of the most carefully worked out dose-response relationships is that for carbon monoxide poisoning. Based on controlled studies of exposure in humans at low levels and on observations in humans who have suffered high level exposures because of their occupation or because of accidents or suicide attempts, the relationship between blood levels of carboxyhemoglobin (COHb) and toxicity is understood as follows ... 

No studies were located regarding death in humans after oral exposure to heptachlor or heptachlor epoxide. However, since heptachlor is a major component of the insecticide chlordane, chlordane poisoning can be considered when evaluating heptachlor toxicity data. In the case study of a woman who ingested 6 g of chlordane with suicidal intent and died 9.5 days following ingestion, no information was presented on the composition of the chlordane. Therefore, the amount of heptachlor exposure is unknown, and the effect of other components of chlordane cannot be ruled out (Derbes et al. 1955). 

Death. Occupational mortality studies of pesticide workers exposed to heptachlor have not revealed an excess number of deaths in these cohorts compared to the general U.S. population. This may possibly be explained as a healthy worker effect. The ERA has described human case reports in which convulsions and death were reported following suicidal ingestion of technical-grade chlordane, which typically contains 6-30% heptachlor, but these effects cannot be attributed to heptachlor or heptachlor epoxide. There are no controlled, quantitative human data for any route of exposure. Acute lethality data were located for animals exposed via the oral and dermal routes. Both heptachlor and heptachlor epoxide may be considered very toxic via the oral route on the basis of acute animal data in rats and mice. Intermediate oral exposure to these compounds also caused up to 40% and 100% mortality in rats and mice, respectively. There appear to be differences in sensitivity in males and females in some species with the males being most sensitive. Heptachlor epoxide is more toxic than heptachlor. Heptachlor may be considered very toxic to extremely toxic via the dermal route on the basis of acute lethality data in rats and mice. The severity of acute effects may possibly depend upon the extent of formation of heptachlor epoxide and the species tested. 

In 1960, Dr. Sidney Cohen s meta-analysis of 25,000 LSD exposures (derived from a large number of published reports) indicated a surprisingly low incidence of flashbacks and a very low rate of suicide. Almost all of them occurred soon after LSD use suicides thereafter tended to reflect the incidence in the general population. 

Case reports describe a particular effect observed in an individual or a group of individuals in which an exposure to a substance has occurred, often accidentally or in suicidal attempts. Information can be obtained from published case reports or from poison information centers. 

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